Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0000737 (abdominal pain)
 31,184 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synthetic cyclic growth-hormone release-inhibiting hormone (G.H.-R.I.H.) impaired platelet aggregation in each of four healthy men given 6-hour infusions. The effects lasted over 24 hours in three of them. There was no consistent change in platelet-counts during the infusions, but 18 hours after the end of the infusions there was a slight but significant increase in platelet-count. There was no change in prothrombin-time, partial thromboplastin-time, fibrinogen titres, and fibrinogen-degradation products. Incubation of G.H.-R.I.H. with blood in vitro did not affect platelet aggregation. Similar impairment of platelet function has been reported by others in baboons given linear G.H.-R.I.H. Infusions in the four healthy men studied also produced abdominal pain, dizziness, and diarrhoea in three, as have been reported in patients similarly infused. Although other side-effects or impairment of platelet-counts or bleeding-tendencies have not been reported in patients infused for up to 72 hours, caution should be exercised when using G.H.-R.I.H. over extended periods until further data on its toxicity are available.
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PMID:Impairment of platelet function by growth-hormone release-inhibiting hormone. 4 78

A stroma-free hemoglobin (SFH) solution was prepared which was sterile, pyrogen free, and contained only 1.2% of the stromal lipid present in unpurified hemolysate, 250 ml of which was administered slowly intravenously to 8 healthy men. Two control subjects received 250 ml of serum albumin. The SFH infusions were generally well tolerated by 7 of the 8 men. One subject developed abdominal pain and costovertebral angle tenderness after infusion, which disappeared within 48 hr. Bradycardia and a mild increase in blood pressure was present during ths SFH infusions and for 4 to 5 hr thereafter. A decrease in urine output and endogenous creatinine clearance appeared during the SFH infusions and for 2 to 4 hr after infusion. A mild prolongation of the activated partial thromboplastin time developed immediately after infusion. Gross hemoglobinuria appeared as expected during the SFH infusions and completely disappeared by 6 to 10 hr after infusion. All the cardiovascular, renal, and clotting changes were present for only a few hours after the SFH infusion, during the hemoglobinemia (free Hb in plasma). At 24 hr and 7 days after infusion all measurements were normal, and 6 mo follow-up showed no abnormalities or hepatitis.
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PMID:A clinical safety trial of stroma-free hemoglobin. 61 11

Fifteen Thai children, diagnosed with dengue hemorrhagic fever and admitted to the Children's Hospital in Bangkok, were studied. All cases were serologically proved to be secondary dengue infections. The clinical signs and symptoms in the first few days of the acute febrile phase were similar to those observed in cases with classical dengue fever, and included continuously high fever, headache, muscle pain, nausea, vomiting and abdominal pain, etc. In the laboratory findings we noted hypoalbuminemia and mild elevation of the GOT and GPT. The hemogram showed an increasing atypical lymphocyte count during the acute febrile period. Prolongations of the partial thromboplastin time and thrombin time were also found, especially in the severe shock cases. All patients had varying degrees of hepatomegaly and pleural effusion from their chest x-rays accompanied by a rapid increase in the hematocrit of more than 20% and a fall in the platelet count to less than 100000/microliters. During the plasma leakage period the patients easily developed shock, even leading to death, unless adequate fluid supplies were given. This is also the major pathophysiological difference between dengue hemorrhagic fever and classical dengue fever. Although some studies concerning the pathogenesis of dengue hemorrhagic fever have been reported, but the exact mechanisms need further investigation.
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PMID:[Clinical observation of 15 Thai children with dengue hemorrhagic fever]. 234 55

A polyethylene glycol conjugate of L-asparaginase (PEGLA) was administered to 21 patients with refractory non-Hodgkin's lymphoma. The dose given was 2,000 mu/m2 intramuscularly every 2 weeks. Eligibility required at least one prior trial of chemotherapy and ambulatory performance status. At entry, all patients had measurable lesions and documented disease progression. The median age of the patients was 61 years; 18 (86%) were ambulatory with minimal symptoms, 12 patients (57%) had 3 or more prior regimens, and 13 (62%) had stage IV disease. Histologic subtype was low grade in 11 patients (52%), intermediate in 7 (33%), high grade in 2 (10%) and unclassifiable in one (5%). There were two partial responses (11%) noted (95% confidence interval of response of 1-30%). Eleven patients (52%) were removed from study due to disease progression. Nine patients (43%), required removal for toxicity (7 for protracted nausea and vomiting and 2 for confusion). One patient died of sepsis while on study but this was not considered drug related. Almost one third of patients complained of fatigue or loss of appetite. Nausea and vomiting occurred in approximately half the patients and was moderate to severe in 9. Diarrhea and abdominal pain were also noted in one-third of those treated. Changes in the partial thromboplastin time and fibrinogen were noted in most patients but resulted in no bleeding complications. In this trial, PEGLA displayed modest activity in a heterogenous group of patients with progressive non-Hodgkin's lymphoma.
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PMID:A phase II trial of PEG-L-asparaginase in the treatment of non-Hodgkins lymphoma. 234 67

Free perforation occurred in only 7 of 702 patients with ulcerative colitis (1 percent) without toxic dilatation seen at The Mount Sinai Hospital from 1960 to 1981; however, these seven patients represented 30 percent (7 of 23) of all colonic perforations seen in patients with ulcerative colitis in our institution during the same period. Classic physical signs of peritonitis (silent, rigid abdomen and rebound tenderness) were absent in six of the seven patients, but all had a marked deterioration in general condition after perforation. Other signs included a sudden increase in severity of abdominal pain (three patients), marked abdominal distention (four patients), and a sharp decrease in frequency of bowel movements (six patients). Mortality was high (four of seven patients, 57 percent) and characterized by comparatively longer patient histories of colitis, longer current attacks, slightly greater delays between presumed perforation and operation, much higher transfusion requirements, and a 100 percent incidence of coagulopathy (thrombocytopenia and increased prothrombin time in three of four patients, and increased partial thromboplastin time in all four patients). The possibility of free perforation in ulcerative colitis must be considered in fulminating cases, even in the absence of colonic dilatation. Careful clinical monitoring and early surgical intervention may be the keys to reducing mortality.
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PMID:Free colonic perforation without dilatation in ulcerative colitis. 375 75

Lupus anticoagulant is an immunoglobulin that interferes with prothrombin conversion to thrombin and is manifested biochemically by prolongation of the partial thromboplastin time. Paradoxically, bleeding is rare in association with this anticoagulant, and deep leg vein thromboses, pulmonary emboli, and cerebrovascular accidents have been described in patients with this clotting inhibitor. This report describes the first case of Budd-Chiari syndrome associated with the lupus anticoagulant. The patient presented with abdominal pain and massive ascites. The Budd-Chiari syndrome was confirmed by liver biopsy and venography. No medical condition known to predispose to an increased thrombotic tendency could be identified, and the presence of the lupus anticoagulant in the patient's plasma may provide an explanation for his hypercoagulability and development of the Budd-Chiari syndrome.
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PMID:Budd-Chiari syndrome in a patient with the lupus anticoagulant. 641 18

Intramural hematoma of the small intestine is a relatively rare but serious complication of oral anticoagulant therapy. On the basis of a retrospective epidemiological survey the authors estimate its incidence at 1 case per 20 000 admissions to medical and surgical services or 1 case per 2500 anticoagulated patients per year. The classical trial of clinical symptoms comprises abdominal pain, small bowel obstruction and multiple hemorrhagic symptoms (hematuria, hematomas, ecchymoses, hematemesis and melaena). The most important etiologic factors appear to be overanticoagulation with vitamin K antagonists (the thromboplastin time is prolonged in over 70% of cases) or correct oral anticoagulation associated with additional impairment of hemostasis due to the administration of drugs inhibiting platelet function. Radiologic examination of the gastrointestinal tract reveals that the jejunum and the ileum are sites of predilection for intramural intestinal hematoma. The treatment of choice is conservative; surgery should be reserved for cases in which the diagnosis is doubtful and for patients who exhibit signs of bowel necrosis or peritonitis.
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PMID:[Incidence of intramural digestive system hematoma in anticoagulation. Epidemiologic study and clinical aspects of 59 cases observed in Switzerland (1970-1975)]. 660 15

Sixty-seven cases of eclampsia were managed between August 1977 and July 1980. Routinely acquired laboratory tests of these cases have been analyzed. In addition, the group of patients with eclampsia was compared with a group of 24 healthy pregnant women. There was no significant difference in platelet count, serum fibrinogen, and bilirubin values. The activated partial thromboplastin time was abnormal in 42% of patients with eclampsia. There was no clinical evidence of disseminated intravascular coagulation in any patient. Patients with eclampsia had abnormalities of lactic dehydrogenase, alkaline phosphatase, SGOT, uric acid, BUN, and creatinine. However, in any individual patients there was no single test of great clinical usefulness and no test predictive of maternal or fetal outcome. At present the authors recommend complete blood count (including blood smear and platelet count), clot observation, and serum creatinine tests. Liver function tests are reserved for the patient with upper abdominal pain. Additional tests are recommended if the diagnosis of eclampsia is questionable or if an additional disease process is suspected.
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PMID:Eclampsia II. Clinical significance of laboratory findings. 707 59

Intravenous injection of crude marijuana extract led to development of an acute illness with multisystem involvement. Gastrointestinal manifestations consisted of severe vomiting, diarrhea, and crampy abdominal pain. Hypotension, tachycardia, and peripheral vasodilation constituted the main cardiovascular manifestations of the disease. Moderate azotemia and oliguria, presumed to be of prerenal origin, were present and rapidly resolved with administration of intravenous fluids. Hematologic manifestations consisted of leukocytosis with a left shift, thrombocytopenia, prolonged partial thromboplastin time, increased fibrin degradation products, and positive protamine sulfate test. The observed coagulation abnormalities may suggest intravascular coagulation. C3, C4, and total hemolytic complement were reduced, suggesting possible activation of the complement system. Hyperventilation, hypoxemia, pulmonary edema, obstructive, and restrictive pulmonary function abnormalities and bilateral pleural effusions highlighted the pulmonary manifestations of the disease. Rhadbomyolysis and mild hepatic function abnormalities were also present. All observed abnormalities reversed in a few days with no significant sequelae.
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PMID:Toxicity with intravenous injection of crude marijuana extract. 723 64

Acute intrinsic renal failure was diagnosed in a two-year-old, male, German shepherd dog following a Vipera aspis bite. Clinical signs included depression, hypersalivation, vomiting, tachypnoea, abdominal pain, splenomegaly, oliguria with haematuria and haemolysed serum. Leucocytosis with a shift to the left, thrombocytopenia, prolonged coagulation times (activated partial thromboplastin time, prothrombin time and thrombin time), hypofibrinogenaemia, azotaemia and hyposthenuria were the most prominent laboratory abnormalities. Histopathological evaluation of the kidneys showed a discrete glomerular hypercellularity, mesangial lysis and renal tubules filled with many hyaline casts and some necrotic cells.
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PMID:Acute intrinsic renal failure and blood coagulation disorders after a snakebite in a dog. 747 66


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